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A 34-year-old man was admitted with acute lung injury and COVID-19 pneumonia. In intensive care unit, he experienced episodes of prolonged asystole accompanied by hypotension without loss of consciousness. Once reversible causes were excluded, symptoms were related to dysfunction of the sinus node and patient underwent PM implantation., Graphical abstract

The sick sinus syndrome includes symptoms and signs related to sinus node dysfunction. This can be caused by intrinsic abnormal impulse formation and/or propagation from the sinus node or, in some cases, by extrinsic reversible causes. Careful evaluation of symptoms and of the electrocardiogram is of crucial importance, because diagnosis is mainly based on these 2 elements. In some cases, the pathophysiologic mechanism that induces sinus node dysfunction also favors the onset of atrial arrhythmias, which results in a more complex clinical condition, known as "bradycardia-tachycardia syndrome."

The hearts of seven elderly dogs in which bradycardia-tachycardia syndrome (BTS) had been diagnosed electrocardiographically were examined post mortem. The clinical basis of the underlying heart disease was invariably mitral or mitral and tricuspid regurgitation. Microscopical examination of the sinoatrial (SA) node and the SA junctional region consistently revealed depletion of SA nodal cells, with a corresponding increase in fibrous or fibro-fatty tissue that interrupted contiguity between the SA node and the surrounding atrial myocardium. The left and right atrial walls showed an increased amount of fibrous tissue in the myocardium and disruption of the muscle bundle architecture (interstitial myocardial fibrosis) to varying degrees. Qualitatively, these changes in the SA node and the SA node region resembled those associated with ageing in elderly people with or without BTS. Thus, it is possible that the pathological process affecting the SA node in these dogs was fundamentally related to ageing and may have caused BTS, in combination with atrial myocardial lesions caused by mitral and tricuspid regurgitation.

The management of bradycardia-tachycardia syndrome (BTS) includes bradycardia and tachyarrhythmia therapy. At present, the treatment for symptomatic bradycardia in BTS patients is permanent cardiac pacing. The pharmacological treatment of atrial tachyarrhythmias comprises of rhythm and rate control, and prevention of thromboembolism. Patients with BTS often require both pacemaker and drug therapy. This article reviews the interactions of pacing and drug therapies in BTS. Drugs that alter cardiac electrophysiological properties may influence pacemaker indications, pacing mode selection, efficacy of pacing algorithms and pacing performance. Pacing by preventing drug-induced bradycardia increases the safety of pharmacotherapy and, thus, allows the intensification of those treatments. Pacing therapy and antiarrhythmic drugs used together as a hybrid therapy have a synergistic effect in the prevention of atrial tachyarrhythmias. Atrial-based pacing may reduce atrial tachyarrhythmia burden, allowing reduction of rhythm and rate control. Contemporary pacemakers' memory functions may help guide rhythm and rate control, as well as anticoagulation pharmacotherapy.

INTRODUCTION Biatrial pacing is expected to have preventive effects on atrial fibrillation. METHODS We evaluated atrial regional wall motion by strain Doppler imaging (SDI) in 6 patients (62.5 +/- 11.3 [SD] years), who suffered from atrial fibrillation, with an implanted biatrial pacemaker. SDI was performed and atrial regional wall motion was estimated during biatrial (BiA) and right atrial appendage (RAA) pacing. RESULTS There was no significant difference in the interval from the pacing spike to the peak strain of the atrium in the lateral right atrium (LRA) between BiA and RAA pacing. However, there was a significant difference in the septal atrium (SA) between BiA and RAA pacing (225.0 +/- 19.9 vs 267.2 +/- 15.7 ms, P < 0.0001) and in the lateral left atrium (LLA) between BiA and RAA pacing (216.7 +/- 21.6 vs 275.0 +/- 16.2 ms, P < 0.0001). There were significant differences in the time difference of peak strain between BiA and RAA pacing in each atrial segment (LRA-AS: 2.2 +/- 5.9 vs 45.0 +/- 11.9 ms, P = 0.0016, SA-LLA: -8.3 +/- 5.5 vs 7.8 +/- 2.7 ms, P < 0.0011, LRA-LLA: -6.1 +/- 3.9 vs 52.8 +/- 13.2 ms, P = 0.0002). There was no significant difference in the interval from the pacing spike to the inflection point of atrial strain (S-I) of LRA. However, there were significant differences in S-I of SA (83.9 +/- 24.1 vs 129.9 +/- 30.6 ms, P = 0.0086) and LLA (102.2 +/- 37.9 vs 166.1 +/- 13.4 ms, P = 0.0028). CONCLUSION BiA pacing improved the synchronicity of regional wall motion of both atrium.

The authors present a patient with carbamazepine-induced bradycardia-tachycardia syndrome, a rare type of drug-induced sinus node dysfunction. In this case, they established a clear-cut relationship between plasma carbamazepine concentration and the frequency of sinus arrests, following episodes of supraventricular tachycardia. As the pharmacological analysis of drug-induced sinus node dysfunction by concurrent ECG monitoring is very limited, the findings give an insight into the mechanism of this disorder.

SCHWABB, B., et al.: AAIR Versus DDDR Pacing in the Bradycardia Tachycardia Syndrome: A Prospective, Randomized, Double-blind, Crossover Trial. In 19 patients paced and medicated for bradycardia tachycardia syndrome (BTS), AAIR and DDDR pacing were compared with regard to quality of life (QoL), atrial tachyarrhythmia (AFib), exercise tolerance, and left ventricular (LV) function. Patients had a PQ interval ≤ 240 ms during sinus rhythm, no second or third degree AV block, no bundle branch block, or bifascicular block. In DDDR mode, AV delay was optimized using the aortic time velocity integral. After 3 months, QoL was assessed by questionnaires, patients were investigated by 24-hour Holter, cardiopulmonary exercise testing (CPX) was performed, and LV function was determined by echocardiography. QoL was similar in all dimensions, except dizziness, showing a significantly lower prevalence in AAIR mode. The incidence of AFib was 12 episodes in 2 patients with AAIR versus 22 episodes in 7 patients with DDDR pacing (P = 0.072). In AAIR mode, 164 events of second and third degree AV block were detected in 7 patients (37%) with pauses between 1 and 4 seconds. During CPX, exercise duration and work load were higher in AAIR than in DDDR mode (423 ± 127 vs 402 ± 102 s and 103 ± 31 vs 96 ± 27 Watt, P < 0.05). Oxygen consumption (VO2), was similar in both modes. During echocardiography, only deceleration of early diastolic flow velocity and early diastolic closure rate of the anterior mitral valve leaflet were higher in DDD than in AAI pacing (5.16 ± 1.35 vs 3.56 ± 0.95 m/s2 and 69.2 ± 23 vs 54.1 ± 26 mm/s, P < 0.05). As preferred pacing mode, 11 patients chose DDDR, 8 patients chose AAIR. Hence, AAIR and DDDR pacing seem to be equally effective in BTS patients. In view of a considerable rate of high degree AV block during AAIR pacing, DDDR mode should be preferred for safety reasons.

The bradycardia-tachycardia syndrome is a subgroup within the larger category of sinus node dysfunction. Pacing is often required to treat either the protracted asystolic spells following the spontaneous termination of a paroxysmal supra-ventricular tachyarhythmia or to protect the patient from pharmacologically exacerbated bradycardias. While the optimal pacing mode for this subset of patients remains debatable, recent reports have favored the use of atrial ventricular sequential pacing with intact atrial sensing (DDI). This paper reports our experience with a series of 30 consecutive patients in whom the DDI mode was utilized as part of the management of this syndrome. DDI pacing has been demonstrated to be safe, extremely effective, and easy to use in this group of patients.

4 patients with the bradycardia-tachycardia syndrome have been treated for 4–13 months with amiodarone at a daily dose of 200 mg for 5–6 days every week. After this treatment was started neither episo

Five patients with the bradycardia-tachycardia syndrome have been treated successfully with the antiarrhythmic agent amiodarone. Three patients were treated for over nine months and one of these patients had corneal micro deposits. One patient had to be taken off the drug because of side effects. Amiodarone should be tried in patients suffering from the bradycardia-tachycardia syndrome before resorting to cardiac pacing.

The bradycardia-tachycardia syndrome (paroxysmal supraventricular tachycardia alternating with sinus bradycardia and episodes of sinus node arrest) has previously presented a complicated therapeutic dilemma when excitatory and suppressive drugs have been utilized. A patient with this syndrome successfully treated with a permanent ventricular transvenous demand pacemaker is presented. Various aspects of this syndrome as well as facets of diagnosis and treatment have been reviewed and discussed. Significant underlying cardiac disease was ruled out in this patient by the usual diagnostic methods including left heart catheterization and coronary angiography. An interesting possibility of the relationship of vagal stimulation secondary to hiatus hernia as an etiologic factor in this syndrome has been discussed. The opinion is expressed that the currently preferred method of treatment is the insertion of a permanent transvenous pacemaker alone or in conjunction with antiarrhythmic drugs, preferably digitalis and propranolol.

The clinical spectrum of the sick sinus syndrome (SSS) is described in a series of 56 patients who demonstrated either persistent unexplained sinus bradycardia (group I: eight patients); sinus arrest (group II: 15 patients); or bradycardia with episodic supraventricular tachyarrhythmias (group III: 33 patients). Coronary disease was the most common form of heart disease where etiology could be determined, but in 25 patients no clear etiologic diagnoses could be established. Thirty-three patients showed associated electrocardiographic conduction disturbances. Symptoms were common and were produced by both bradycardia and tachycardia. Eight patients in the bradycardia-tachycardia group experienced cerebral embolization. Despite bother-some symptoms, only six of the 56 patients died over an average follow-up of 7 years, and only one of these deaths appeared related to an arrhythmia. Drug therapy of bradycardia was generally ineffective, but digitalis was frequently helpful in patients with tachycardia. Electrical pacing was uniformly successful in treating symptoms of bradycardia but was disappointing in preventing tachyarrhythmias.

Thirty-one patients with the bradycardia-tachycardia syndrome treated with permanent ventricular pacemakers were studied. All were symptomatic before pacemaker insertion, and their symptoms were not controlled with drug therapy alone. Bradycardia and tachycardia associated with multiple arrhythmias were present in all cases; heart rate was less than 40 beats/min in 58 percent of patients and more than 140 beats/min in 71 percent. Conduction abnormalities were present in 61 percent. After insertion of a demand pacemaker, 27 patients (87 percent) were symptom-free for 1 month to 5 years. Although four patients with a normally functioning pacemaker continued to have recurrent arrhythmia, the presence of a pacemaker facilitated further pharmacologic treatment of the disturbance. Pacemaker insertion has been found to be a satisfactory method of treating the symptoms and preventing the recurrence of arrhythmias in patients with the bradycardia-tachycardia syndrome by allowing the use of digitalis and other antiarrhythmic agents.

Permanent pacing in children, including those with postoperative bradycardia-tachycardia syndrome, has been compromised by the availability of pulse generators, electrode leads and implantation techniques designed for the adult patient. Recent technologic improvements and simplified implantation techniques have reduced many of these barriers and have made endocardial as well as epicardial ventricular pacing more feasible. However, in some children, ventricular pacing may be impeded by anatomic abnormalities due to congenital anomalies or prior cardiac operations. In these instances, endocardial atrial pacing may provide an alternative therapeutic approach in selected patients. This report describes the use of endocardial atrial demand pacing in four children with postoperative bradycardia-tachycardia syndrome and restricted ventricular access. This approach controls symptomatic bradycardia, helps prevent and convert paroxysmal intraatrial tachycardia and overcomes the problem of limited ventricular access.

In a patient with Wolff-Parkinson-White syndrome, transient normalization of the QRS complex occurred as a result of retrograde concealed conduction into the accessory pathway from an A-V junctional escape beat. This patient also had a bradycardia-tachycardia syndrome.

A 75-year-old woman was admitted to the hospital because of a supraventricular tachycardia, long sinus pauses and ventricular tachycardia of the torsades de pointe type. Temporary ventricular pacing suppressed ventricular arrhythmias but supraventricular tachy-cardia persisted. An electrophysiologic study revealed the coexistence of sick sinus syndrome and cir-cus movement tachycardia due to a concealed left-sided accessory atrioventricular pathway. This case represents a previously undescribed form of the bradycardia-tachycardia syndrome. (PACE, Vol. 5, July-August, 1982)

A 17-year-old patient is discussed who had the tachycardia-bradycardia syndrome following closure of a sinus venosus atrial septal defect. Cardiac standstill up to 7.2 seconds long occurred, but placement of a permanent demand pacemaker was avoided. This unique case demonstrates that permanent pacemaker may not always be necessary in the tachycardia-bradycardia syndrome, especially when it occurs in a young postsurgical patient.